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Phenotype for activated tissue macrophages in histiocytic necrotizing lymphadenitis
Author(s) -
Nomura Yuko,
Takeuchi Masanori,
Yoshida Shiro,
Sugita Yasuo,
Niino Daisuke,
Kimura Yoshizo,
Shimizu Kei,
Aoki Ryosuke,
Suefuji Nobuko,
Hirose Shinichi,
Kikuchi Masahiro,
Ohshima Koichi
Publication year - 2009
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2009.02418.x
Subject(s) - ccl22 , cd68 , c c chemokine receptor type 7 , chemokine , cd163 , pathology , macrophage polarization , macrophage , biology , immunology , chemokine receptor , immunohistochemistry , medicine , inflammation , in vitro , biochemistry
Macrophage polarization is divided into M1 and M2 type based on membrane receptors, cytokines, and chemokines. M1 expresses CD80, interleukin (IL)‐6, IL‐12, and chemokine receptor (CCR)7, while M2 expresses CD163, IL10, and chemokine ligand (CCL)22. The aim of the present study was to identify the properties of infiltrating tissue macrophages in histiocytic necrotizing lymphadenitis (HNL). Twenty patients with HNL were studied, and immunohistochemistry for CD68 (KP1), CD163, CCL22, CCR7, and CD123 was done, along with myeloperoxidase (MPO). To evaluate the phenotypes of tissue macrophages in HNL, the number of cells stained positively for CD163, CCL22, CCR7, CD123 and MPO concurrently with CD68 was counted, and the ratio was calculated for each antibody to CD68+ cells. There was a high rate of co‐expression for CD163 (median, 78%) or CCL22 (80%) and a low rate for CCR7 (5%) in CD68+ cells. It is therefore conceivable that infiltration by M2 macrophages is dominant in HNL. Furthermore, some CD68+ tissue macrophages in HNL co‐express MPO or CD123 (range, 5–80%; median, 23% and 40%, respectively). It is suggested that these characteristic tissue macrophages may be associated with the pathogenesis of HNL and that M2 macrophages may infiltrate to repair the lymphoid tissue injured by cytotoxic T cells in HNL.